Direct Myocardial Damage Research Articles

Ritmo nodal secundario a descarga eléctrica de alto voltaje: Report of one case

Electrical shock can cause a direct myocardial damage and different types of arrhythmias, which are uncommon and occur more often when there is a high voltage exposure. We report a 19-year-old male that received a high voltage shock, falling thereafter from an altitude of four meters. On admission to the emergency room, he had second and third degree burns in the right hand and the left thigh. The electrocardiogram showed a nodal rhythm of 72 beats per minute. After four hours of monitoring, sinus rhythm returned spontaneously.

Myocardial infarction secondary to electrocution: report of a child case

Cardiac rhythm defects can be seen due to electrocution related injuries. However, myocardial infarcts due to electrocution are rarely seen. Here, we present a case of myocardial infarction due to electrocution in children, with its medico-legal aspects. A thirteen years old male exposed to electrical current while playing with an open electrical cable. He was arrested upon admission to the emergency department. Laboratory tests revealed cardiac affection characterized with increased levels of cardiac enzymes and troponin. Three days after injury the child died in intensive care unit. At autopsy, entry and exit points of electrical injuries were seen on right and left hands. Histopathological examination showed finding attributable to myocardial infarction. Myocardial infarction due to electrocution is generally caused by coronary artery vasospasm and/or direct myocardial damage. Crime scene investigation findings, hospital records are of high importance to be available and such documents should be reviewed prior to autopsy. Furthermore, photographing of injuries and histopathological evaluation of skin lesions should be performed.

Parvovirus-Mediated Fetal Cardiomyopathy With Atrioventricular Nodal Disease

Acute parvovirus B19 infection (API) in pregnancy has been associated with fetal anemia and hydrops fetalis. Direct myocardial damage from API in a fetus and an infant has been described. This report presents a case of fetal second-degree heart block and cardiomyopathy secondary to API. A 19-year-old G4P1112 (gravida 4 para 2 with 1 term delivery, 1 preterm delivery, 1 termination, and 2 living children) was referred at 20 weeks gestation for fetal bradycardia. A 2:1 atrioventricular block was identified by fetal echocardiography at 23 weeks. Hydrops developed at 25 weeks. Amniocentesis and percutaneous umbilical blood sampling demonstrated API. At 31 weeks, the patient presented with preterm labor and delivered a viable female infant, who died of poor cardiac function and arrhythmia on the first day of life. In addition to fetal anemia and hydrops fetalis, API in pregnancy may cause direct fetal myocardial damage and conduction system disease.

Transient left midventricular ballooning without apical involvement

We present a case of a 51-years-old woman with acute chest pain and ECG showing diffuse ST segment deviation who was transferred to our hospital to perform an urgent coronary angiography. There were no significant obstructions and left ventriculography (LVG) showed a midventricular ballooning without the apical dysynergy described previously in Tako-Tsubo or stress-induced cardiomyopathy. She had a favourable hospital course and a new LVG at 30 days showed total normalization of contractility. This recently described new pattern of transient left ventricular dysfunction was probably induced by a great mental stress state that the patient described in the preceding 24–48 h and the intrinsic mechanism could be a direct catecholamine myocardial damage or a microcirculation spasm.

Expression of costimulatory molecules B7-1, B7-2, and CD40 in the heart of patients with acute myocarditis and dilated cardiomyopathy.

In patients with acute myocarditis and dilated cardiomyopathy (DCM), we previously reported that antigen-specific T cells infiltrate the heart and play an important role in the myocardial damage involved. For antigen-specific T-cell activation to occur, it is necessary for T cells to receive a costimulatory signal provided by costimulatory molecules expressed on antigen-presenting cells (APCs) as well as the main signal provided by binding of T-cell receptors to the antigen. To investigate the roles of the costimulatory molecules B7-1, B7-2, and CD40 in the development of acute myocarditis and DCM, we analyzed the expression of these antigens in the myocardial tissues of patients with acute myocarditis and DCM. We also examined the expression of a cytolytic factor, perforin, in the infiltrating cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells, because both killer lymphocytes are thought to damage B7-1-expressing APCs. We found that B7-1, B7-2, and CD40 were moderately to strongly expressed in the cardiac myocytes of patients with acute myocarditis. Weak to moderate expression of these antigens was also found in the cardiac myocytes of patients with DCM. There was infiltration of perforin-expressing CTLs and NK cells in the myocardial tissues of patients with acute myocarditis and DCM. Our findings strongly suggest that expression of B7-1, B7-2, and CD40 antigens on cardiac myocytes may make them APCs for CTLs and NK cells and that they may play an important role in the direct myocardial damage by these killer cells in acute myocarditis and DCM.

The Monitoring of Potential Long-Term Complications in Treated Adult Cancer Patients

A wide variety of long-term complications may be noted following conventional cancer treatment. These include overwhelming postsplenectomy sepsis syndrome, central and peripheral nervous system toxicity, cardiovascular complications, chronic liver damage, and secondary malignancy. Follow-up monitoring usually incorporates both physical examination and the result of radiological and laboratory investigations. Primary care physicians will often be responsible for the majority of the follow-up monitoring involving cured cancer patients and need to be aware of possible long-term therapy-related problems, especially those that present years after successful treatment of the original malignancy.

Use of the Isolated Perfused Heart for Evaluation of Cardiac Toxicity

The isolated perfused rat heart model can be used to evaluate cardiotoxicity, and is especially useful in distinguishing direct vs indirect cardiac injury. Various perfusion systems can be used to characterize the pathophysiologic as well as morphologic changes induced by drugs or chemicals of interest. The isolated perfused heart was used in the studies described herein to characterize the mechanism of allylamine cardiotoxicity. Rat hearts were perfused with Krebs-Henseleit buffer containing 10 mM allylamine and a latex balloon was inserted into the left ventricle to monitor pressure. Coronary flow in hearts perfused with 10 mM allylamine was similar to control hearts at 5, 10, and 30 min, but was reduced by 1 hr (11.5 +/- 0.6 ml/min/g wet heart weight vs 16.0 +/- 0.7, p less than 0.01). Peak left ventricular systolic pressure increased in hearts perfused with allylamine for 5 min (156 +/- 8 mm Hg vs 103 +/- 9, p less than 0.01), but by 2 hr was decreased compared to controls (89 +/- 6 vs 105 +/- 5, p less than 0.05). End diastolic pressure was markedly increased at 2 hr (58 +/- 3 vs 4 +/- 0.8, p less than 0.01). Morphologically, allylamine perfused hearts exhibited significant contraction band changes as well as numerous cells with marked swelling of the sarcoplasmic reticulum. The findings in this study suggest that allylamine produces direct myocardial damage that appears to be independent of coronary flow. These studies demonstrate that the isolated perfused rat heart model can be used to evaluate mechanisms of acute cardiotoxicity.

Cardiac isoenzymes and electrocardiographic changes during ritodrine tocolysis

To investigate the potential myocardial ischemic effects of ritodrine, we studied 36 singleton and four twin preterm pregnancies during ritodrine therapy. We serially determined serum creatinine phosphokinase (CPK-MB fraction) and lactic dehydrogenase isoenzymes and performed electrocardiography before and during ritodrine infusion and again within the first 24 hours of oral drug therapy. We observed that serum CPK-MB and lactic dehydrogenase isoenzymes remained within the normal range during therapy periods. The incidence of sinus tachycardia and non-specific T wave changes were 100% and 25%, respectively. In three of four twin pregnancies, ST-T segment depression in leads I, V 4, V 5, and V 6 of the electrocardiogram was noted. Our study suggests that (1) the recommended ritodrine regimen does not produce direct myocardial damage, and (2) ritodrine may cause cardiac ischemia as determined by electrocardiography, which theoretically would progress to myocardial damage if not treated properly.

Effect of interferon, interleukin-2 and tumor necrosis factor on myocardial cell viability and doxorubicin cardiotoxicity in vitro

Neonatal rat heart myocytes were cultured in plastic 24-well plates for 6 days over which time ATP and protein levels steadily increased. Synchronous beating rates of 40–50 per min are obtained 3 days after plating 1.14 × 106 myocytes/well. The addition of rat interferon (IFN) or recombinant human interleukin (IL-2) or tumor necrosis factor (TNF) at concentrations of 10–1000 U/ml for 24–48 h did not reduce ATP/protein ratios or significantly affect beating rates. A 6-h exposure to doxorubicin concentrations of 0.5 μg/ml and 1.0 μg/ml reduced control ATP/protein ratios of 6.8–7.3 ng/gmg by 78% and 40%, respectively. Importantly, the addition of 100 U/ml of IL-2, TNF or IFN to these doxorubicin concentrations did not alter doxorubicin-induced cardiotoxicity. These results suggest that IL-2, TNF and IFN do not cause direct myocardial cell damage and may be cautiously combined with doxorubicin without enhanced cardiotoxic effects. The reported cardiotoxicity from such cytokines may be principally due to peripheral vascular effects which reflexly stress the heart.

Membrane damage and the pathogenesis of cardiomyopathies

Membrane damage plays an important role in the pathogenesis of ischemic damage to the myocardium, and is ultimately responsible for the release of cellular contents notably intracellular enzymes after ischemic cell death. This membrane damage may be caused by the incorporation of lipids into myocardial membranes, by the enzymatic actions of lipases that hydrolyze membrane phospholipids, and by free radicals that are produced in the ischemic myocardium. Much less is known of the role of membrane damage in the cardiomyopathies, but direct myocardial membrane damage may occur in some specific forms of this diverse class of diseases. Direct membrane effects of exogenous substances are likely to be of pathogenic significance in alcoholic and some toxic cardiomyopathies, for example those produced by hydrocarbons and adriamycin. Membrane damage may also play a role in the pathogenesis of viral cardiomyopathies, due possibly to incorporation of viral components into the cardiac sarcolemma where these foreign materials can serve as antigens that direct host responses to attack the cells of the heart.